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* Levodopa: This drug is the most effective in controlling motor symptoms in [[Parkinson's disease|PD]] patients.<ref name="pmid24756517">{{cite journal |vauthors=Connolly BS, Lang AE |title=Pharmacological treatment of Parkinson disease: a review |journal=JAMA |volume=311 |issue=16 |pages=1670–83 |date=2014 |pmid=24756517 |doi=10.1001/jama.2014.3654 |url=}}</ref><ref name="pmid23279439">{{cite journal |vauthors=Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G, Dietrichs E, Fabbrini G, Friedman A, Kanovsky P, Kostic V, Nieuwboer A, Odin P, Poewe W, Rascol O, Sampaio C, Schüpbach M, Tolosa E, Trenkwalder C, Schapira A, Berardelli A, Oertel WH |title=Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease |journal=Eur. J. Neurol. |volume=20 |issue=1 |pages=5–15 |date=January 2013 |pmid=23279439 |doi=10.1111/j.1468-1331.2012.03866.x |url=}}</ref> If we use [[levodopa]] alone, it will convert to [[dopamine]] in the peripheral circulation, so we combine it with a decarboxylase inhibitor like [[carbidopa]] to prevent this. The ratio of carbidopa_levodopa in tablets are 10/100, 25/100 or 25/250.<ref name="pmid15706700">{{cite journal |vauthors= |title=Parcopa: a rapidly dissolving formulation of carbidopa/levodopa |journal=Med Lett Drugs Ther |volume=47 |issue=1201 |pages=12 |date=January 2005 |pmid=15706700 |doi= |url=}}</ref><ref name="pmid20925074">{{cite journal |vauthors=Ondo WG, Shinawi L, Moore S |title=Comparison of orally dissolving carbidopa/levodopa (Parcopa) to conventional oral carbidopa/levodopa: A single-dose, double-blind, double-dummy, placebo-controlled, crossover trial |journal=Mov. Disord. |volume=25 |issue=16 |pages=2724–7 |date=December 2010 |pmid=20925074 |doi=10.1002/mds.23158 |url=}}</ref> The [[adverse effects]] of this drug includes elevated serum [[homocysteine]], low levels of [[vitamin B12]], elevated [[methylmalonic acid]] and sensorimotor peripheral neuropathy.<ref name="pmid18785232">{{cite journal |vauthors=Toth C, Brown MS, Furtado S, Suchowersky O, Zochodne D |title=Neuropathy as a potential complication of levodopa use in Parkinson's disease |journal=Mov. Disord. |volume=23 |issue=13 |pages=1850–9 |date=October 2008 |pmid=18785232 |doi=10.1002/mds.22137 |url=}}</ref><ref name="pmid20582991">{{cite journal |vauthors=Toth C, Breithaupt K, Ge S, Duan Y, Terris JM, Thiessen A, Wiebe S, Zochodne DW, Suchowersky O |title=Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease |journal=Ann. Neurol. |volume=68 |issue=1 |pages=28–36 |date=July 2010 |pmid=20582991 |doi=10.1002/ana.22021 |url=}}</ref><ref name="pmid23836370">{{cite journal |vauthors=Ceravolo R, Cossu G, Bandettini di Poggio M, Santoro L, Barone P, Zibetti M, Frosini D, Nicoletti V, Manganelli F, Iodice R, Picillo M, Merola A, Lopiano L, Paribello A, Manca D, Melis M, Marchese R, Borelli P, Mereu A, Contu P, Abbruzzese G, Bonuccelli U |title=Neuropathy and levodopa in Parkinson's disease: evidence from a multicenter study |journal=Mov. Disord. |volume=28 |issue=10 |pages=1391–7 |date=September 2013 |pmid=23836370 |doi=10.1002/mds.25585 |url=}}</ref><ref name="pmid25168395">{{cite journal |vauthors=Uncini A, Eleopra R, Onofrj M |title=Polyneuropathy associated with duodenal infusion of levodopa in Parkinson's disease: features, pathogenesis and management |journal=J. Neurol. Neurosurg. Psychiatry |volume=86 |issue=5 |pages=490–5 |date=May 2015 |pmid=25168395 |doi=10.1136/jnnp-2014-308586 |url=}}</ref> It can also cause motor fluctuations, [[dyskinesia]], [[cramps]] and [[dystonia]].<ref name="pmid20880751">{{cite journal |vauthors=Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B |title=Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap |journal=Lancet Neurol |volume=9 |issue=11 |pages=1106–17 |date=November 2010 |pmid=20880751 |doi=10.1016/S1474-4422(10)70218-0 |url=}}</ref><ref name="pmid25488260">{{cite journal |vauthors=Aquino CC, Fox SH |title=Clinical spectrum of levodopa-induced complications |journal=Mov. Disord. |volume=30 |issue=1 |pages=80–9 |date=January 2015 |pmid=25488260 |doi=10.1002/mds.26125 |url=}}</ref> One of the concerns regarding long term use of [[levodopa]] is that it may be increase the rate of [[dopamine]] [[Neuron|neurons]] degeneration<ref name="pmid15372588">{{cite journal |vauthors=Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Bonucelli U, Damier P, De Yebenes J, Gershanik O, Guttman M, Grandas F, Hallett M, Hornykiewicz O, Jenner P, Katzenschlager R, Langston WJ, LeWitt P, Melamed E, Mena MA, Michel PP, Mytilineou C, Obeso JA, Poewe W, Quinn N, Raisman-Vozari R, Rajput AH, Rascol O, Sampaio C, Stocchi F |title=Levodopa in the treatment of Parkinson's disease: current controversies |journal=Mov. Disord. |volume=19 |issue=9 |pages=997–1005 |date=September 2004 |pmid=15372588 |doi=10.1002/mds.20243 |url=}}</ref> but other studies demonstrated  that it does not damage [[Neuron|neurons]].<ref name="pmid11553992">{{cite journal |vauthors=Rajput AH |title=The protective role of levodopa in the human substantia nigra |journal=Adv Neurol |volume=86 |issue= |pages=327–36 |date=2001 |pmid=11553992 |doi= |url=}}</ref><ref name="pmid21917769">{{cite journal |vauthors=Parkkinen L, O'Sullivan SS, Kuoppamäki M, Collins C, Kallis C, Holton JL, Williams DR, Revesz T, Lees AJ |title=Does levodopa accelerate the pathologic process in Parkinson disease brain? |journal=Neurology |volume=77 |issue=15 |pages=1420–6 |date=October 2011 |pmid=21917769 |doi=10.1212/WNL.0b013e318232ab4c |url=}}</ref>
* Levodopa: This drug is the most effective in controlling motor symptoms in [[Parkinson's disease|PD]] patients.<ref name="pmid24756517">{{cite journal |vauthors=Connolly BS, Lang AE |title=Pharmacological treatment of Parkinson disease: a review |journal=JAMA |volume=311 |issue=16 |pages=1670–83 |date=2014 |pmid=24756517 |doi=10.1001/jama.2014.3654 |url=}}</ref><ref name="pmid23279439">{{cite journal |vauthors=Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G, Dietrichs E, Fabbrini G, Friedman A, Kanovsky P, Kostic V, Nieuwboer A, Odin P, Poewe W, Rascol O, Sampaio C, Schüpbach M, Tolosa E, Trenkwalder C, Schapira A, Berardelli A, Oertel WH |title=Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease |journal=Eur. J. Neurol. |volume=20 |issue=1 |pages=5–15 |date=January 2013 |pmid=23279439 |doi=10.1111/j.1468-1331.2012.03866.x |url=}}</ref> If we use [[levodopa]] alone, it will convert to [[dopamine]] in the peripheral circulation, so we combine it with a decarboxylase inhibitor like [[carbidopa]] to prevent this. The ratio of carbidopa_levodopa in tablets are 10/100, 25/100 or 25/250.<ref name="pmid15706700">{{cite journal |vauthors= |title=Parcopa: a rapidly dissolving formulation of carbidopa/levodopa |journal=Med Lett Drugs Ther |volume=47 |issue=1201 |pages=12 |date=January 2005 |pmid=15706700 |doi= |url=}}</ref><ref name="pmid20925074">{{cite journal |vauthors=Ondo WG, Shinawi L, Moore S |title=Comparison of orally dissolving carbidopa/levodopa (Parcopa) to conventional oral carbidopa/levodopa: A single-dose, double-blind, double-dummy, placebo-controlled, crossover trial |journal=Mov. Disord. |volume=25 |issue=16 |pages=2724–7 |date=December 2010 |pmid=20925074 |doi=10.1002/mds.23158 |url=}}</ref> The [[adverse effects]] of this drug includes elevated serum [[homocysteine]], low levels of [[vitamin B12]], elevated [[methylmalonic acid]] and sensorimotor peripheral neuropathy.<ref name="pmid18785232">{{cite journal |vauthors=Toth C, Brown MS, Furtado S, Suchowersky O, Zochodne D |title=Neuropathy as a potential complication of levodopa use in Parkinson's disease |journal=Mov. Disord. |volume=23 |issue=13 |pages=1850–9 |date=October 2008 |pmid=18785232 |doi=10.1002/mds.22137 |url=}}</ref><ref name="pmid20582991">{{cite journal |vauthors=Toth C, Breithaupt K, Ge S, Duan Y, Terris JM, Thiessen A, Wiebe S, Zochodne DW, Suchowersky O |title=Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease |journal=Ann. Neurol. |volume=68 |issue=1 |pages=28–36 |date=July 2010 |pmid=20582991 |doi=10.1002/ana.22021 |url=}}</ref><ref name="pmid23836370">{{cite journal |vauthors=Ceravolo R, Cossu G, Bandettini di Poggio M, Santoro L, Barone P, Zibetti M, Frosini D, Nicoletti V, Manganelli F, Iodice R, Picillo M, Merola A, Lopiano L, Paribello A, Manca D, Melis M, Marchese R, Borelli P, Mereu A, Contu P, Abbruzzese G, Bonuccelli U |title=Neuropathy and levodopa in Parkinson's disease: evidence from a multicenter study |journal=Mov. Disord. |volume=28 |issue=10 |pages=1391–7 |date=September 2013 |pmid=23836370 |doi=10.1002/mds.25585 |url=}}</ref><ref name="pmid25168395">{{cite journal |vauthors=Uncini A, Eleopra R, Onofrj M |title=Polyneuropathy associated with duodenal infusion of levodopa in Parkinson's disease: features, pathogenesis and management |journal=J. Neurol. Neurosurg. Psychiatry |volume=86 |issue=5 |pages=490–5 |date=May 2015 |pmid=25168395 |doi=10.1136/jnnp-2014-308586 |url=}}</ref> It can also cause motor fluctuations, [[dyskinesia]], [[cramps]] and [[dystonia]].<ref name="pmid20880751">{{cite journal |vauthors=Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B |title=Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap |journal=Lancet Neurol |volume=9 |issue=11 |pages=1106–17 |date=November 2010 |pmid=20880751 |doi=10.1016/S1474-4422(10)70218-0 |url=}}</ref><ref name="pmid25488260">{{cite journal |vauthors=Aquino CC, Fox SH |title=Clinical spectrum of levodopa-induced complications |journal=Mov. Disord. |volume=30 |issue=1 |pages=80–9 |date=January 2015 |pmid=25488260 |doi=10.1002/mds.26125 |url=}}</ref> One of the concerns regarding long term use of [[levodopa]] is that it may be increase the rate of [[dopamine]] [[Neuron|neurons]] degeneration<ref name="pmid15372588">{{cite journal |vauthors=Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Bonucelli U, Damier P, De Yebenes J, Gershanik O, Guttman M, Grandas F, Hallett M, Hornykiewicz O, Jenner P, Katzenschlager R, Langston WJ, LeWitt P, Melamed E, Mena MA, Michel PP, Mytilineou C, Obeso JA, Poewe W, Quinn N, Raisman-Vozari R, Rajput AH, Rascol O, Sampaio C, Stocchi F |title=Levodopa in the treatment of Parkinson's disease: current controversies |journal=Mov. Disord. |volume=19 |issue=9 |pages=997–1005 |date=September 2004 |pmid=15372588 |doi=10.1002/mds.20243 |url=}}</ref> but other studies demonstrated  that it does not damage [[Neuron|neurons]].<ref name="pmid11553992">{{cite journal |vauthors=Rajput AH |title=The protective role of levodopa in the human substantia nigra |journal=Adv Neurol |volume=86 |issue= |pages=327–36 |date=2001 |pmid=11553992 |doi= |url=}}</ref><ref name="pmid21917769">{{cite journal |vauthors=Parkkinen L, O'Sullivan SS, Kuoppamäki M, Collins C, Kallis C, Holton JL, Williams DR, Revesz T, Lees AJ |title=Does levodopa accelerate the pathologic process in Parkinson disease brain? |journal=Neurology |volume=77 |issue=15 |pages=1420–6 |date=October 2011 |pmid=21917769 |doi=10.1212/WNL.0b013e318232ab4c |url=}}</ref>
* Dopamine agonists: [[Dopamine agonist]] such as [[bromocriptine]], [[pramipexole]] and [[ropinirole]] are proved to be effective in managing motor symptoms of [[Parkinson's disease|PD]] patients.<ref name="pmid11402154">{{cite journal |vauthors=Olanow CW, Watts RL, Koller WC |title=An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines |journal=Neurology |volume=56 |issue=11 Suppl 5 |pages=S1–S88 |date=June 2001 |pmid=11402154 |doi= |url=}}</ref> At first, the use of [[dopamine agonist]] were limited t the condition where there is reduced [[levodopa]] response or when we had disturbing [[levodopa]] [[complications]]<ref name="pmid8959987">{{cite journal |vauthors=Fahn S |title=Is levodopa toxic? |journal=Neurology |volume=47 |issue=6 Suppl 3 |pages=S184–95 |date=December 1996 |pmid=8959987 |doi= |url=}}</ref><ref name="pmid3341935">{{cite journal |vauthors= |title=International symposium on early dopamine agonist therapy of Parkinson's disease |journal=Arch. Neurol. |volume=45 |issue=2 |pages=204–8 |date=February 1988 |pmid=3341935 |doi= |url=}}</ref> but since [[dopamine agonist]]<nowiki/>s have fewer [[Side effects|side effects,]] some experts suggest using these drugs as the first line therapy especially for [[Parkinson's disease|PD]] patients under 60 years old.<ref name="pmid18490620">{{cite journal |vauthors=Marras C, Lang A |title=Invited article: changing concepts in Parkinson disease: moving beyond the decade of the brain |journal=Neurology |volume=70 |issue=21 |pages=1996–2003 |date=May 2008 |pmid=18490620 |doi=10.1212/01.wnl.0000312515.52545.51 |url=}}</ref> The [[adverse effects]] of [[dopamine agonist]] are [[nausea]], [[vomiting]], sleep disorders, [[confusion]], [[peripheral edema]] and [[valvular heart disease]].<ref name="pmid18425954">{{cite journal |vauthors=Stowe RL, Ives NJ, Clarke C, van Hilten J, Ferreira J, Hawker RJ, Shah L, Wheatley K, Gray R |title=Dopamine agonist therapy in early Parkinson's disease |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD006564 |date=April 2008 |pmid=18425954 |doi=10.1002/14651858.CD006564.pub2 |url=}}</ref><ref name="pmid17202450">{{cite journal |vauthors=Roth BL |title=Drugs and valvular heart disease |journal=N. Engl. J. Med. |volume=356 |issue=1 |pages=6–9 |date=January 2007 |pmid=17202450 |doi=10.1056/NEJMp068265 |url=}}</ref>
* Dopamine agonists: [[Dopamine agonist]] such as [[bromocriptine]], [[pramipexole]] and [[ropinirole]] are proved to be effective in managing motor symptoms of [[Parkinson's disease|PD]] patients.<ref name="pmid11402154">{{cite journal |vauthors=Olanow CW, Watts RL, Koller WC |title=An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines |journal=Neurology |volume=56 |issue=11 Suppl 5 |pages=S1–S88 |date=June 2001 |pmid=11402154 |doi= |url=}}</ref> At first, the use of [[dopamine agonist]] were limited t the condition where there is reduced [[levodopa]] response or when we had disturbing [[levodopa]] [[complications]]<ref name="pmid8959987">{{cite journal |vauthors=Fahn S |title=Is levodopa toxic? |journal=Neurology |volume=47 |issue=6 Suppl 3 |pages=S184–95 |date=December 1996 |pmid=8959987 |doi= |url=}}</ref><ref name="pmid3341935">{{cite journal |vauthors= |title=International symposium on early dopamine agonist therapy of Parkinson's disease |journal=Arch. Neurol. |volume=45 |issue=2 |pages=204–8 |date=February 1988 |pmid=3341935 |doi= |url=}}</ref> but since [[dopamine agonist]]<nowiki/>s have fewer [[Side effects|side effects,]] some experts suggest using these drugs as the first line therapy especially for [[Parkinson's disease|PD]] patients under 60 years old.<ref name="pmid18490620">{{cite journal |vauthors=Marras C, Lang A |title=Invited article: changing concepts in Parkinson disease: moving beyond the decade of the brain |journal=Neurology |volume=70 |issue=21 |pages=1996–2003 |date=May 2008 |pmid=18490620 |doi=10.1212/01.wnl.0000312515.52545.51 |url=}}</ref> The [[adverse effects]] of [[dopamine agonist]] are [[nausea]], [[vomiting]], sleep disorders, [[confusion]], [[peripheral edema]] and [[valvular heart disease]].<ref name="pmid18425954">{{cite journal |vauthors=Stowe RL, Ives NJ, Clarke C, van Hilten J, Ferreira J, Hawker RJ, Shah L, Wheatley K, Gray R |title=Dopamine agonist therapy in early Parkinson's disease |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD006564 |date=April 2008 |pmid=18425954 |doi=10.1002/14651858.CD006564.pub2 |url=}}</ref><ref name="pmid17202450">{{cite journal |vauthors=Roth BL |title=Drugs and valvular heart disease |journal=N. Engl. J. Med. |volume=356 |issue=1 |pages=6–9 |date=January 2007 |pmid=17202450 |doi=10.1056/NEJMp068265 |url=}}</ref>
* Monoamine oxidase (MAO) B inhibitors: [[MAO inhibitors|MAO B inhibitors]] such as [[selegiline]], [[rasagiline]] and safinamide are proved to be helpful in managing motor symptoms of [[Parkinson's disease|PD]] patients.(99_100_101_102_103_104) these drugs can cause [[nausea]] and [[headaches]].(100) [[Rasagiline]] can also cause impulse control disorders.(116)
* Monoamine oxidase (MAO) B inhibitors: [[MAO inhibitors|MAO B inhibitors]] such as [[selegiline]], [[rasagiline]] and safinamide are proved to be helpful in managing motor symptoms of [[Parkinson's disease|PD]] patients.<ref name="pmid8959990">{{cite journal |vauthors=Olanow CW |title=Selegiline: current perspectives on issues related to neuroprotection and mortality |journal=Neurology |volume=47 |issue=6 Suppl 3 |pages=S210–6 |date=December 1996 |pmid=8959990 |doi= |url=}}</ref><ref name="pmid15477585">{{cite journal |vauthors=Horn S, Stern MB |title=The comparative effects of medical therapies for Parkinson's disease |journal=Neurology |volume=63 |issue=7 Suppl 2 |pages=S7–12 |date=October 2004 |pmid=15477585 |doi= |url=}}</ref><ref name="pmid12470183">{{cite journal |vauthors= |title=A controlled trial of rasagiline in early Parkinson disease: the TEMPO Study |journal=Arch. Neurol. |volume=59 |issue=12 |pages=1937–43 |date=December 2002 |pmid=12470183 |doi= |url=}}</ref><ref name="pmid15096406">{{cite journal |vauthors= |title=A controlled, randomized, delayed-start study of rasagiline in early Parkinson disease |journal=Arch. Neurol. |volume=61 |issue=4 |pages=561–6 |date=April 2004 |pmid=15096406 |doi=10.1001/archneur.61.4.561 |url=}}</ref> these drugs can cause [[nausea]] and [[headaches]].<ref name="pmid15477585">{{cite journal |vauthors=Horn S, Stern MB |title=The comparative effects of medical therapies for Parkinson's disease |journal=Neurology |volume=63 |issue=7 Suppl 2 |pages=S7–12 |date=October 2004 |pmid=15477585 |doi= |url=}}</ref> [[Rasagiline]] can also cause impulse control disorders.<ref name="pmid23305965">{{cite journal |vauthors=Vitale C, Santangelo G, Erro R, Errico D, Manganelli F, Improta I, Moccia M, Barone P |title=Impulse control disorders induced by rasagiline as adjunctive therapy for Parkinson's disease: report of 2 cases |journal=Parkinsonism Relat. Disord. |volume=19 |issue=4 |pages=483–4 |date=April 2013 |pmid=23305965 |doi=10.1016/j.parkreldis.2012.11.008 |url=}}</ref>
* Anticholinergic agents:
* Anticholinergic agents:
* Amantadine:  
* Amantadine:  

Revision as of 13:48, 20 April 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Medical Therapy

The mainstay of therapy for motor symptoms of Parkinson disease are:

Treatment choices for some of the nonmotor symptoms of PD are:

  • Psychosis:
  • Dementia:
  • Daytime sleepiness:
  • Fatigue:
  • Depression:
  • Constipation:
  • Sialorrhea:
  • Rhinorrhea:
  • Sexual dysfunction:
  • Ortostatic hypotention:

References

  1. Connolly BS, Lang AE (2014). "Pharmacological treatment of Parkinson disease: a review". JAMA. 311 (16): 1670–83. doi:10.1001/jama.2014.3654. PMID 24756517.
  2. Ferreira JJ, Katzenschlager R, Bloem BR, Bonuccelli U, Burn D, Deuschl G, Dietrichs E, Fabbrini G, Friedman A, Kanovsky P, Kostic V, Nieuwboer A, Odin P, Poewe W, Rascol O, Sampaio C, Schüpbach M, Tolosa E, Trenkwalder C, Schapira A, Berardelli A, Oertel WH (January 2013). "Summary of the recommendations of the EFNS/MDS-ES review on therapeutic management of Parkinson's disease". Eur. J. Neurol. 20 (1): 5–15. doi:10.1111/j.1468-1331.2012.03866.x. PMID 23279439.
  3. "Parcopa: a rapidly dissolving formulation of carbidopa/levodopa". Med Lett Drugs Ther. 47 (1201): 12. January 2005. PMID 15706700.
  4. Ondo WG, Shinawi L, Moore S (December 2010). "Comparison of orally dissolving carbidopa/levodopa (Parcopa) to conventional oral carbidopa/levodopa: A single-dose, double-blind, double-dummy, placebo-controlled, crossover trial". Mov. Disord. 25 (16): 2724–7. doi:10.1002/mds.23158. PMID 20925074.
  5. Toth C, Brown MS, Furtado S, Suchowersky O, Zochodne D (October 2008). "Neuropathy as a potential complication of levodopa use in Parkinson's disease". Mov. Disord. 23 (13): 1850–9. doi:10.1002/mds.22137. PMID 18785232.
  6. Toth C, Breithaupt K, Ge S, Duan Y, Terris JM, Thiessen A, Wiebe S, Zochodne DW, Suchowersky O (July 2010). "Levodopa, methylmalonic acid, and neuropathy in idiopathic Parkinson disease". Ann. Neurol. 68 (1): 28–36. doi:10.1002/ana.22021. PMID 20582991.
  7. Ceravolo R, Cossu G, Bandettini di Poggio M, Santoro L, Barone P, Zibetti M, Frosini D, Nicoletti V, Manganelli F, Iodice R, Picillo M, Merola A, Lopiano L, Paribello A, Manca D, Melis M, Marchese R, Borelli P, Mereu A, Contu P, Abbruzzese G, Bonuccelli U (September 2013). "Neuropathy and levodopa in Parkinson's disease: evidence from a multicenter study". Mov. Disord. 28 (10): 1391–7. doi:10.1002/mds.25585. PMID 23836370.
  8. Uncini A, Eleopra R, Onofrj M (May 2015). "Polyneuropathy associated with duodenal infusion of levodopa in Parkinson's disease: features, pathogenesis and management". J. Neurol. Neurosurg. Psychiatry. 86 (5): 490–5. doi:10.1136/jnnp-2014-308586. PMID 25168395.
  9. Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B (November 2010). "Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap". Lancet Neurol. 9 (11): 1106–17. doi:10.1016/S1474-4422(10)70218-0. PMID 20880751.
  10. Aquino CC, Fox SH (January 2015). "Clinical spectrum of levodopa-induced complications". Mov. Disord. 30 (1): 80–9. doi:10.1002/mds.26125. PMID 25488260.
  11. Olanow CW, Agid Y, Mizuno Y, Albanese A, Bonuccelli U, Bonucelli U, Damier P, De Yebenes J, Gershanik O, Guttman M, Grandas F, Hallett M, Hornykiewicz O, Jenner P, Katzenschlager R, Langston WJ, LeWitt P, Melamed E, Mena MA, Michel PP, Mytilineou C, Obeso JA, Poewe W, Quinn N, Raisman-Vozari R, Rajput AH, Rascol O, Sampaio C, Stocchi F (September 2004). "Levodopa in the treatment of Parkinson's disease: current controversies". Mov. Disord. 19 (9): 997–1005. doi:10.1002/mds.20243. PMID 15372588.
  12. Rajput AH (2001). "The protective role of levodopa in the human substantia nigra". Adv Neurol. 86: 327–36. PMID 11553992.
  13. Parkkinen L, O'Sullivan SS, Kuoppamäki M, Collins C, Kallis C, Holton JL, Williams DR, Revesz T, Lees AJ (October 2011). "Does levodopa accelerate the pathologic process in Parkinson disease brain?". Neurology. 77 (15): 1420–6. doi:10.1212/WNL.0b013e318232ab4c. PMID 21917769.
  14. Olanow CW, Watts RL, Koller WC (June 2001). "An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines". Neurology. 56 (11 Suppl 5): S1–S88. PMID 11402154.
  15. Fahn S (December 1996). "Is levodopa toxic?". Neurology. 47 (6 Suppl 3): S184–95. PMID 8959987.
  16. "International symposium on early dopamine agonist therapy of Parkinson's disease". Arch. Neurol. 45 (2): 204–8. February 1988. PMID 3341935.
  17. Marras C, Lang A (May 2008). "Invited article: changing concepts in Parkinson disease: moving beyond the decade of the brain". Neurology. 70 (21): 1996–2003. doi:10.1212/01.wnl.0000312515.52545.51. PMID 18490620.
  18. Stowe RL, Ives NJ, Clarke C, van Hilten J, Ferreira J, Hawker RJ, Shah L, Wheatley K, Gray R (April 2008). "Dopamine agonist therapy in early Parkinson's disease". Cochrane Database Syst Rev (2): CD006564. doi:10.1002/14651858.CD006564.pub2. PMID 18425954.
  19. Roth BL (January 2007). "Drugs and valvular heart disease". N. Engl. J. Med. 356 (1): 6–9. doi:10.1056/NEJMp068265. PMID 17202450.
  20. Olanow CW (December 1996). "Selegiline: current perspectives on issues related to neuroprotection and mortality". Neurology. 47 (6 Suppl 3): S210–6. PMID 8959990.
  21. 21.0 21.1 Horn S, Stern MB (October 2004). "The comparative effects of medical therapies for Parkinson's disease". Neurology. 63 (7 Suppl 2): S7–12. PMID 15477585.
  22. "A controlled trial of rasagiline in early Parkinson disease: the TEMPO Study". Arch. Neurol. 59 (12): 1937–43. December 2002. PMID 12470183.
  23. "A controlled, randomized, delayed-start study of rasagiline in early Parkinson disease". Arch. Neurol. 61 (4): 561–6. April 2004. doi:10.1001/archneur.61.4.561. PMID 15096406.
  24. Vitale C, Santangelo G, Erro R, Errico D, Manganelli F, Improta I, Moccia M, Barone P (April 2013). "Impulse control disorders induced by rasagiline as adjunctive therapy for Parkinson's disease: report of 2 cases". Parkinsonism Relat. Disord. 19 (4): 483–4. doi:10.1016/j.parkreldis.2012.11.008. PMID 23305965.

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